Purpose: Motor deficits after stroke are supposed to arise from the reduced neural drive from the brain to muscles. This study aimed to demonstrate the feasibility of reflecting the motor function improvement after stroke with the measurement of corticomuscular coherence (CMC) in an individual subject.
Method: A stroke patient was recruited to participate in an experiment before and after the function recovery of his paretic upper limb, respectively. An elbow flexion task with a constant muscle contraction level was involved in the experiment. Electromyography and electroencephalography signals were recorded simultaneously to estimate the CMC. The non-parameter statistical analysis was used to test the significance of CMC differences between the first and second times of experiments.
Result: The strongest corticomuscular coupling emerged at the motor cortex contralateral to the contracting muscles for both the affected and unaffected limbs. The strength of the corticomuscular coupling between activities from the paretic limb muscles and the contralateral motor cortex for the second time of experiment increased significantly compared with that for the first time. However, the CMC of the unaffected limb had no significant changes between two times of experiments.
Conclusion: The results demonstrated that the increased corticomuscular coupling strength resulted from the motor function restoration of the paretic limb. The measure of CMC can reflect the recovery of motor function after stroke by quantifying interactions between activities from the motor cortex and controlled muscles.
Stroke is one of the major diseases that cause long-term motor deficits of adults (1). However, our poor understanding of the mechanisms underlying motor impairments after stroke limits greatly the development of effective intervention and evaluation methods. In general, motor impairments after stroke are deemed to arise from changes in both neural and muscle properties. Poststroke changes in the neural system have been studied from different points of view such as the decreased excitability of the affected cortex (2, 3) and the increased inhibitory effect from the unaffected hemisphere on the affected hemisphere (4). Spasm and flaccid paresis of muscles are believed to result from the loss of control input from the brain at different phases after stroke. Even though stroke survivors have been demonstrated to have significant descending information flow in the affected side during the chronic period (5), there is evidence that poststroke impairments reflect the reduced central neural drive to muscles. Mima et al. and Fang et al. found that the functional coupling between cortical commands and consequent muscle activities of stroke subjects were weaker than that of healthy controls (6, 7). The conduction time from the central cortical rhythm to peripheral oscillations in the affected side was significantly prolonged compared with that of the unaffected side after stroke (8).
It is believed that stroke interrupts the motor-related neural network and then reduces the neural drive to the muscles. The coherent activities between the motor cortex and the muscles are believed to reflect the synchronized discharge of corticospinal cells (9). It can be estimated by analyzing the frequency domain coherence (10) between electromyography (EMG) and electroencephalography (EEG) signals termed as corticomuscular coherence (CMC). Although previous studies have demonstrated that the CMC strength of poststroke subjects was weaker than that of healthy controls, it is still not clear whether the corticomuscular coupling will enhance along with the motor function recovery to directly reflect the motor function state of paretic limbs after stroke. In the current study, a poststroke patient was recruited to participate in two times of experiments involving an elbow flexion task. The time interval between two times of experiments was determined to guarantee that the patient had obtained an obvious motor function recovery of the affected upper extremity. CMC from two times of experiments was estimated and compared to verify whether motor function recovery can be reflected by the change of corticomuscular coupling strength.
Experiment and Subject
An elbow flexion task was designed for the stroke patient because only poor rehabilitation outcomes can be generally obtained for hand. The force applied by the elbow flexion was monitored by a strain gage and fed back to the patient visually to help him finish the task with moderate and constant muscle contractions (11), because coherence analyses (12, 13) have demonstrated that the coupling is most pronounced in the beta-band range during steady muscle contractions and the beta-band CMC is assumed to be associated with strategies for controlling submaximal muscle forces (12, 14, 15). The designed motion task and the visual feedback information on screen are illustrated in Figures 1A,B, respectively. A trial was initiated when a circle and a target ring showed on screen and was over when they disappeared. Each trial lasted 11 s and there was a 2-s long interval between adjacent trials. Each run contained 20 trials and each side of upper limbs performed two runs, respectively. The subject practiced before data recording until the target force could be reached within the first 2 s of each trial.